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Interpretation of Arterial Blood Gases (ABGs) David A.

Kaufman, MD Chief, Section of Pulmonary, Critical Care & Sleep Medicine Bridgeport Hospital-Yale New Haven Health Assistant Clinical Professor, Yale University School of Medicine (Section of Pulmonary & Critical Care Medicine) Introduction:

Interpreting an arterial blood gas (ABG) is a crucial skill for physicians, nurses, respiratory therapists, and other health care personnel. ABG interpretation is especially important in critically ill patients. The following six-step process helps ensure a complete interpretation of every ABG. In addition, you will find tables that list commonly encountered acidbase disorders. Many methods exist to guide the interpretation of the ABG. This discussion does not include some methods, such as analysis of base excess or Stewarts strong ion difference. A summary of these techniques can be found in some of the suggested articles. It is unclear whether these alternate methods offer clinically important advantages over the presented approach, which is based on the anion gap. Readers are welcome to discuss their observations and share their comments on the ATS Critical Care Forums.

6-step approach: Step 1: Assess the internal consistency of the values using the Henderseon-Hasselbach equation: [H+] = 24(PaCO2) [HCO3-] If the pH and the [H+] are inconsistent, the ABG is probably not valid.

pH

Approximate [H+] (mmol/L) 100 89 79 71 63 56 50 45

7.00 7.05 7.10 7.15 7.20 7.25 7.30 7.35

7.40 7.45 7.50 7.55 7.60 7.65


Step 2: Is there alkalemia or acidemia present?

40 35 32 28 25 22

pH < 7.35 acidemia pH > 7.45 alkalemia

You will need to check the PaCO2, HCO3- and anion gap Step 3: Is the disturbance respiratory or metabolic? What is the relationship between the direction of change in the pH and the direction of change in the PaCO2? In primary respiratory disorders, the pH and PaCO2 change inopposite directions; in metabolic disorders the pH and PaCO2 change in the same direction.

This is usually the primary disorder Remember: an acidosis or alkalosis may be present even if the pH is in the normal range (7.35 7.45)

Acidosis Acidosis Alkalosis Alkalosis

Respiratory Metabolic& Respiratory Metabolic

pH pH pH pH

PaCO2 PaCO2 PaCO2 PaCO2

Step 4: Is there appropriate compensation for the primary disturbance? Usually, compensation does not return the pH to normal (7.35 7.45).

Disorder

Expected compensation

Correction factor

Metabolic acidosis

PaCO2 = (1.5 x [HCO3-]) +8

Acute respiratory acidosis

Increase in [HCO3-]= PaCO2/10

Chronic respiratory acidosis (3-5 days)

Increase in [HCO3-]= 3.5( PaCO2/10)

Metabolic alkalosis

Increase in PaCO2 = 40 + 0.6(HCO3-)

Acute respiratory alkalosis

Decrease in [HCO3-]= 2( PaCO2/10)

Chronic respiratory alkalosis

Decrease in [HCO3-] = 5( PaCO2/10) to 7( PaCO2/10)

If the observed compensation is not the expected compensation, it is likely that more than one acid-base disorder is present. Step 5: Calculate the anion gap (if a metabolic acidosis exists): AG= [Na+]-( [Cl-] + [HCO3-] )-12 2

A normal anion gap is approximately 12 meq/L. In patients with hypoalbuminemia, the normal anion gap is lower than 12 meq/L; the normal anion gap in patie nts with hypoalbuminemia is about 2.5 meq/L lower for each 1 gm/dL decrease in the plasma albumin concentration (for example, a patient with a plasma albumin of 2.0 gm/dL would be approximately 7 meq/L.) If the anion gap is elevated, consider calculating the osmolal gap in compatible clinical situations.

Elevation in AG is not explained by an obvious case (DKA, lactic acidosis, renal failure Toxic ingestion is suspected

OSM gap = measured OSM (2[Na+] - glucose/18 BUN/2.8

The OSM gap should be < 10 Step 6: If an increased anion gap is present, assess the relationship between the increase in the anion gap and the decrease in [HCO 3-].
Assess the ratio of the change in the anion gap (AG ) to the change in [HCO3-] ([HCO3-]): AG/[HCO3-] This ratio should be between 1.0 and 2.0 if an uncomplicated anion gap metabolic acidosis is present. If this ratio falls outside of this range, then another metabolic disorder is present:

If AG/[HCO3-] > 2.0, then a concurrent metabolic alkalosis is likely to be present. It is important to remember what the expected normal anion gap for your patient should be, by adjusting for hypoalbuminemia (see Step 5, above.) Table 1: Characteristics of acid-base disturbances

If AG/[HCO3-] < 1.0, then a concurrent non-anion gap metabolic acidosis is likely to be present.

Disorder

pH

Primary problem

Compensation

Metabolic acidosis

in HCO3-

in PaCO2

Metabolic alkalosis

in HCO3-

in PaCO2

Respiratory acidosis

in PaCO2

in [HCO3-]

Respiratory alkalosis

in PaCO2

in [HCO3-]

Table 2: Selected etiologies of respiratory acidosis

Airway obstruction - Upper - Lower

COPD asthma other obstructive lung disease

CNS depression Sleep disordered breathing (OSA or OHS) Neuromuscular impairment Ventilatory restriction Increased CO2 production: shivering, rigors, seizures, malignant hyperthermia, hypermetabolism, increased intake of carbohydrates

Incorrect mechanical ventilation settings Table 3: Selected etiologies of respiratory alkalosis


CNS stimulation: fever, pain, fear, anxiety, CVA, cerebral edema, brain trauma, brain tumor, CNS infection Hypoxemia or hypoxia: lung disease, profound anemia, low FiO2 Stimulation of chest receptors: pulmonary edema, pleural effusion, pneumonia, pneumothorax, pulmonary embolus Drugs, hormones: salicylates, catecholamines, medroxyprogesterone, progestins Pregnancy, liver disease, sepsis, hyperthyroidism

Incorrect mechanical ventilation settings Table 4: Selected causes of metabolic alkalosis

Hypovolemia with Cl- depletion

GI loss of H+

Vomiting, gastric suction, villous adenoma, diarrhea with chloride-rich fluid

Renal loss H+ Loop and thiazide diuretics, post-hypercapnia (especially after institution of mechanical ventilation)

Hypervolemia, Cl- expansion

Renal loss of H+: edematous states (heart failure, cirrhosis, nephrotic syndrome), hyperaldosteronism, hypercortisolism, excess ACTH, exogenous steroids, hyperreninemia, severe hypokalemia, renal artery stenosis, bicarbonate administration Table 5: Selected etiologies of metabolic acidosis

Elevated anion gap:

Methanol intoxication Uremia Diabetic ketoacidosisa, alcoholic ketoacidosis, starvation ketoacidosis Paraldehyde toxicity Isoniazid Lactic acidosisa

Type A: tissue ischemia Type B: Altered cellular metabolism

Ethanolb or ethylene glycolb intoxication

a b

Salicylate intoxication Most common causes of metabolic acidosis with an elevated anion gap Frequently associated with an osmolal gap

Normal anion gap: will have increase in [Cl-]

GI loss of HCO3-

Diarrhea, ileostomy, proximal colostomy, ureteral diversion

Renal loss of HCO3proximal RTA carbonic anhydrase inhibitor (acetazolamide)

Renal tubular disease ATN Chronic renal disease Distal RTA Aldosterone inhibitors or absence

NaCl infusion, TPN, NH4+ administration Table 6: Selected mixed and complex acid-base disturbances

Disorder

Characteristics

Selected situations

Respiratory acidosis with metabolic acidosis

in pH in HCO3 in PaCO2

Cardiac arrest Intoxications Multi-organ failure

Respiratory alkalosis with metabolic alkalosis

in pH in HCO3 in PaCO2

Cirrhosis with diuretics Pregnancy with vomiting Over ventilation of COPD

Respiratory acidosis with metabolic alkalosis

pH in normal range in PaCO2, in HCO3-

COPD with diuretics, vomiting, NG suction Severe hypokalemia

Respiratory alkalosis with metabolic acidosis

pH in normal range in PaCO2 in HCO3

Sepsis Salicylate toxicity Renal failure with CHF or pneumonia Advanced liver disease

Metabolic acidosis with metabolic alkalosis

pH in normal range HCO3- normal

Uremia or ketoacidosis with vomiting, NG suction, diuretics, etc.

Suggested additional reading:

Rose, B.D. and T.W. Post. Clinical physiology of acid-base and electrolyte disorders, 5th ed. New York: McGraw Hill Medical Publishing Division, c2001. Fidkowski, C And J. Helstrom. Diagnosing metabolic acidosis in the critically ill: bridging the anion gap, Stewart and base excess methods. Can J Anesth 2009;56:247-256. Adrogu, H.J. and N.E. Madias. Management of life-threatening acid-base disordersfirst of two parts. N Engl J Med 1998;338:26-34. Adrogu, H.J. and N.E. Madias. Management of life-threatening acid-base disorderssecond of two parts. N Engl J Med 1998;338:107-111.